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Cardiac involvement in Anderson-Fabry disease

Anderson-Fabry disease results from hereditary deficiency of the lysosomal enzyme α-galactosidase A. This disease is marked by progressive intracellular accumulation of globotriaosylceramide (Gb3) and digalactosylceramide, the major glycosphingolipid substrates of α-galactosidase A. Many cell

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Bibliographic Details
Main Authors: Kampmann, Christoph (Author) , Baehner, Frank (Author) , Ries, Markus (Author) , Beck, Michael (Author)
Format: Article (Journal)
Language:English
Published: June 2002
In: Journal of the American Society of Nephrology
Year: 2002, Volume: 13, Pages: S147-S149
ISSN:1533-3450
DOI:10.1097/01.ASN.0000015238.98011.AF
Online Access:Verlag, Volltext: https://doi.org/10.1097/01.ASN.0000015238.98011.AF
Verlag, Volltext: https://jasn.asnjournals.org/content/13/suppl_2/S147
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Author Notes:Christoph Kampmann, Frank Baehner, Markus Ries, and Michael Beck
Description
Summary:Anderson-Fabry disease results from hereditary deficiency of the lysosomal enzyme α-galactosidase A. This disease is marked by progressive intracellular accumulation of globotriaosylceramide (Gb3) and digalactosylceramide, the major glycosphingolipid substrates of α-galactosidase A. Many cell
Item Description:Gesehen am 16.05.2019
Physical Description:Online Resource
ISSN:1533-3450
DOI:10.1097/01.ASN.0000015238.98011.AF

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